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- Title
Nucleotide sequence of chicken c-myb complementary DNA and implications for myb oncogene activation.
- Authors
Rosson, Dan; Reddy, E. Premkumar
- Abstract
Avian myeloblastosis virus (AMV), like other acute transforming viruses, arose by recombination between its helper virus and host cellular sequences. The latter sequences, termed v-myb, are responsible for the oncogenic properties of the virus. AMY causes acute myeloblastic leukaemia in chickens and transforms a specific class of haematopoietic cells in vitro, but does not induce morphological transformation of cultured fibroblasts, suggesting that only a restricted target-cell population is responsive to its transforming gene product1,2. The normal cellular counterpart of v-myb, c-myb, is highly conserved and is present in all vertebrate and some invertebrate species examined3,4. DNA rearrangements and altered expression of the myb oncogene have been reported in mouse lymphoid tumours5-7 and human myeloid8 and colon tumours9. The mechanism of activation of the cellular proto-oncogenes is thought to involve the structural alteration of the coding regions that result in either the synthesis of an altered gene product or the enhanced expression of a proto-oncogene caused by alterations in its regulatory elements. To distinguish between these two mechanisms, we have cloned and sequenced the chicken c-myb complementary DNA and compared it with that of v-myb sequences. We demonstrate that during the transduction of the cellular sequences and/or viral passage a substantial portion of the coding region of the c-myb gene has been lost from both the 5′ and 3′ ends, resulting in the generation of a truncated gene product that mediates the transforming function of the virus.
- Publication
Nature, 1986, Vol 319, Issue 6054, p604
- ISSN
0028-0836
- Publication type
Article
- DOI
10.1038/319604a0